PATTERNS OF THALAMOCORTICAL DEGENERATION AFTER ABLATION OF SOMATOSENSORY CORTEX IN MONKEYS

Citation
J. Chmielowska et Tp. Pons, PATTERNS OF THALAMOCORTICAL DEGENERATION AFTER ABLATION OF SOMATOSENSORY CORTEX IN MONKEYS, Journal of comparative neurology, 360(3), 1995, pp. 377-392
Citations number
29
Categorie Soggetti
Neurosciences
ISSN journal
00219967
Volume
360
Issue
3
Year of publication
1995
Pages
377 - 392
Database
ISI
SICI code
0021-9967(1995)360:3<377:POTDAA>2.0.ZU;2-Q
Abstract
We examined the pattern of cytochrome oxidase (GO), Nissl staining, an d gamma-amino butyric acid (GABA) immunoreactivity in the ventroposter ior lateral nucleus (VPL) of the thalamus in monkeys that received no, total, or subtotal, ablation of the hand representations in postcentr al somatosensory cortex. In unoperated animals, the region of VPL repr esenting the hand was characterized by relatively dense and homogeneou s CO staining throughout the rostral-caudal extent of VPL. Counts of n eurons in the VPL hand representation from adjacent thalamic sections processed for Nissl and GABA immunostaining indicated that there were approximately 261.4 neurons/mm(2) of which 78.4/mm(2) stained positive for GABA. GABA(+) puncta-like terminals were readily apparent through out the VPL. By contrast, animals that received total removals of the postcentral hand representations showed a dramatic reduction in CO sta ining in the VPL, which was confined to the expected location of the t halamic hand representation. Counts of neurons in the affected region from adjacent sections that underwent Nissl staining and GABA immunost aining also revealed a dramatic reduction of Nissl-stained neurons, wi th a smaller reduction in the number of neurons staining positive for GABA. Specifically, large to medium-sized (> 180 mu m(2)) GABA(-) neur ons were virtually eliminated in the affected portion of the VPL, and the numbers of GABA(+) neurons were significantly reduced. The remaini ng population of GABA(+) neurons was typically shrunken, and no GABA() puncta-like terminals were observed in the affected region. The resu lts obtained after subtotal ablation of the postcentral hand represent ations (only one postcentral area spared, 3b or 3a) differed from thos e obtained when total removals were made. Instead of virtually complet e degeneration of medium-sized to large neurons throughout the hand re presentation in VPL, as was the case with total removals, after partia l removals, we found alternating regions in the VPL hand representatio n that appeared qualitatively normal, or dramatically degenerated. Tha lamic sections stained with CO revealed light, moderate, and darkly st ained patches of label within the hand representation in VP, depending on the type of cortical ablation. The most dramatic reduction of Niss l-stained neurons coincided precisely with the lightest staining CO pa tches. Interestingly, the only statistically significant reduction in the number of GABA(+) neurons occurred in the light CO patches. In the thalamic regions coincident with the dark and moderately stained CO p atches, the number of medium-sized and large neurons decreased, but th e number of GABA(+) neurons was comparable to normal. Optical density measurements of the dark patches also indicated a statistically signif icant difference from normal CO staining in this region. These finding s indicate that following cortical damage, complex changes occur in th alamic circuitry. Interestingly, these changes are not confined to reg ions of the thalamus that have their major projection to the damaged r egion of cortex, but include thalamic regions in which the major proje ction is to undamaged regions of cortex. Thus, relatively restricted c ortical damage has the potential to affect regions of cortex not direc tly damaged, through post-injury changes in thalamic circuitry. Such c hanges in neuronal circuitry, especially at the thalamocortical level, may serve as the neural substrate for the limited recovery of behavio ral function often seen after strokes or head injury. (C) 1995 Wiley-L iss, Inc.